Background
Intracranial infection, one of the complications of traumatic brain injury, is usually associated with inflammation. Several microRNAs (miRNAs), including miR-155, have been reported to be critical modulators in peripheral and central nervous system inflammation. In this study, we investigated the role of miR-155 in lipopolysaccharide (LPS)-induced inflammatory injury in mouse microglia BV2 cells.
Conclusions
Knockdown of miR-155 protected mouse microglia BV2 cells from LPS-induced inflammatory injury via targeting RACK1 and deactivating MAPK/NF-κB and mTOR signaling pathways.
Results
The expression level of miR-155 was significantly up-regulated after LPS stimulation in BV2 cells. LPS administration decreased BV2 cell viability, promoted apoptosis and increased the release of pro-inflammatory cytokines; while miR-155 knockdown rescued BV2 cell from LPS-induced injury. RACK1 was a directly target of miR-155. Interestingly, miR-155 knockdown did not attenuate LPS-induced inflammatory injury when RACK1 was knocked down. The mechanistic study indicated that miR-155 knockdown deactivated MAPK/NF-κB and mTOR signaling pathways under LPS-treated conditions. Conclusions: Knockdown of miR-155 protected mouse microglia BV2 cells from LPS-induced inflammatory injury via targeting RACK1 and deactivating MAPK/NF-κB and mTOR signaling pathways.